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Related Concept Videos

Pharmacodynamic Models: Linear Concentration–Effect Model01:15

Pharmacodynamic Models: Linear Concentration–Effect Model

The linear concentration–effect model, underpinned by the principle that pharmacological effect (E) is directly proportional to plasma drug concentration (C), emerges as a pivotal simplification of the Emax model for conditions where C is significantly less than EC50. This model portrays a linear trajectory of the concentration–effect relationship when drug levels are markedly below the EC50 threshold.Despite its inherent assumption of continuous effect augmentation with increasing drug...
Pharmacokinetic–Pharmacodynamic Relationship: Duration of Dose-Effect Relationship01:14

Pharmacokinetic–Pharmacodynamic Relationship: Duration of Dose-Effect Relationship

For drugs producing a quantal response, onset occurs when plasma concentration reaches a minimum effective level (Cmin). The drug's action duration depends on how long the plasma concentration remains above Cmin.Two primary factors influence this duration: dose size and the rate of drug removal from the action site. Both depend on the drug's redistribution to poorly perfused tissues and elimination processes. A larger dose promotes rapid onset and prolongs the effect's duration.Consider a...
Time Course of Drug Effect01:14

Time Course of Drug Effect

The progression of a drug's impact can be analyzed by examining both the concentration-time course and the effect-time course. The concentration-time course is determined by the drug's half-life and is influenced by factors such as its pharmacokinetics, including absorption, distribution, metabolism, and elimination. The effect of the drug is often related to its concentration in the plasma and is calculated using the maximum drug effect and the plasma concentration that generates 50 percent of...
Pharmacokinetic–Pharmacodynamic Relationship: Intensity of Dose-Effect Relationship01:23

Pharmacokinetic–Pharmacodynamic Relationship: Intensity of Dose-Effect Relationship

Pharmacodynamics explores the relationship between drug concentration and its effect. In a quantal response drug, the duration of action better correlates with drug concentration, while for graded effect drugs, the intensity of response is more relevant. This intensity depends on the dose, drug removal rate, and the region of the concentration–response curve.The concentration–response curve can be divided into three regions. Region 3 (80–100% maximum response) demonstrates that even as drug...
Drug Concentration Versus Time Correlation01:15

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The plasma drug concentration-time curve is a crucial tool in pharmacokinetics, representing the drug's concentration in plasma at different time intervals post-administration. This curve illustrates the drug's journey from absorption into the systemic circulation, distribution to body tissues, and eventual elimination through excretion or biotransformation.
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Pharmacodynamic Models: Logarithmic Concentration–Effect Model01:15

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The log-linear model is a pharmacological framework used to describe the relationship between drug concentration and its effect. This model is particularly relevant when the observed effects range between 20% and 80% of the drug’s maximum effect (Emax), where a near-linear relationship is observed between the log of drug concentration and the measured effect. However, the log-linear model does not predict the maximum possible effect (Emax) or the effect at zero drug concentration, limiting its...

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Related Experiment Video

Updated: May 23, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
08:28

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Published on: April 5, 2011

Correlation between plasma quinidine and cardiac effect.

I R Edwards1, B W Hancock, R Saynor

  • 1Academic Division of Medicine, Section of Therapeutics, Royal Infirmary, Sheffield.

British Journal of Clinical Pharmacology
|March 29, 2012
PubMed
Summary
This summary is machine-generated.

The rate of rise in quinidine concentration, not just the level, significantly impacts QTc prolongation. Individual responses to quinidine vary, highlighting potential differences in myocardial sensitivity.

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Area of Science:

  • Pharmacology
  • Cardiology
  • Clinical Medicine

Background:

  • Quinidine is an antiarrhythmic drug known to affect cardiac repolarization.
  • QTc interval prolongation is a potential adverse effect of quinidine therapy.
  • Understanding the relationship between quinidine levels and QTc prolongation is crucial for patient safety.

Purpose of the Study:

  • To assess the relationship between serum quinidine levels and the rate-corrected QT (QTc) interval.
  • To investigate factors influencing QTc prolongation following quinidine administration.
  • To explore individual variability in quinidine response.

Main Methods:

  • Serum quinidine concentrations were measured using a modified Hamfelt & Malers' method.
  • The QTc interval was monitored after administration of single identical quinidine doses.
  • Correlation analysis was performed between quinidine levels, rate of concentration rise, and QTc prolongation.

Main Results:

  • Individual responses in quinidine concentration and QTc prolongation were variable.
  • A significant peak in QTc prolongation occurred post-administration, not always correlating with peak quinidine levels.
  • A stronger correlation (r=0.87) was observed between the rate of quinidine concentration rise and QTc prolongation compared to serum levels (r=0.53).

Conclusions:

  • The rate of increase in serum quinidine concentration is a better predictor of QTc prolongation than the absolute level.
  • Individual variability in response suggests potential differences in myocardial sensitivity to quinidine.
  • Further investigation into factors like red blood cell quinidine levels may elucidate mechanisms of marked QTc prolongation.